I propose to study mammalian behavioral state control through experimental investigations of those mechanisms important for control of the sleep-waking cycle and especially for the desynchronized (d) sleep phase. The guiding theory and organizing principle of this investigation is the reciprocal interaction model of sleep cycle control, which postulates the periodic occurrence of D sleep results from interaction between an excitatory neuronal population in the pontine reticular gigantocellular tegmental field (FTG) and inhibitory neurons in the locus coeruleus (LC, norepinephrine-containing) and dorsaltaphe (serotonin-containing). Intracellular and extracellular recordings of FTG, LC and raphe neurons is unanesthetized cats will critically test the following postulates of this model: An increase in excitability and discharge activity of FTG neurons in permitted to occur when activity in LC/raphe neurons diminishes and FTG neurons are disingibited. Self-excitation in the FTG population leads to a rapid increase in FTG discharge activity and produces a D sleep episode. The D sleep state is terminated when FTG discharge activity recruits sufficient activity in the inhibitory LC/raphe population to suppress FTG activation. The cycle begins again when self-inhibition reduces the level of activity in LC/raphe neuronal populations to the point where FTG cells are again released from inhibition. I propose to develop further the mathematical aspects of the reciprocal interaction model and to test the predictions of its Lotka-Volterra equations about effects on time course of the sleep cycle with localized injection of pharmacologic agents that alter the strength of coupling within and between the neuronal groups of the model. Continued work will be devoted to conceptual and theoretical clarification of the state concept and in particular, to an extension of work linking the physiology of D sleep state with the psychology of the dreaming sleep state.